Ten Years After

When Reactor Number Four at the Chernobyl Nuclear Power Station blew up on April 26, 1986, the explosion sent into the night an invisible army of unknown strength. Over the next several days tons of radioactive debris and particles fell like silent paratroopers onto fields and backyards and streets not only in northern Ukraine, where the explosion happened, but across a wide swath of Europe. Radioactive isotopes infiltrated the food supply and seeped into groundwater.

Ten years after the world’s worst reported nuclear accident, researchers are finding that this insidious, slow-acting enemy is beginning to take a heavy toll. The rates of thyroid cancer in children in parts of Belarus, Russia, and Ukraine are as much as 30 times higher than before the explosion. And equally chilling findings published in 1996 revealed that wildlife and human populations living near Chernobyl suffered genetic damage that they then passed to the next generation. The ultimate consequences of these genetic errors remain a mystery, in part because they’ve never been seen before. Not even radiation from the atomic bombs dropped on Japan during World War II triggered detectable genetic aberrations in children of survivors.

The first onslaught at Chernobyl was not so subtle: one engineer died outright in the explosion, and huge doses of radioactivity killed 28 in the following weeks. The second wave of attack came from iodine 131, a radioactive isotope absorbed by the thyroid gland. Although it has a half- life of only eight days, the isotope still managed to invade the thyroids of vulnerable children, hundreds of whom succumbed to radiation-induced tumors. In the years that have followed, longer-lived radioisotopes like cesium 137, which has a half-life of 30 years and can settle into soil and water, have become the chief threat to health. People are living with this stuff and consuming it, says Sir Alec Jeffreys, a geneticist at the University of Leicester, England.

Jeffreys, an authority on DNA fingerprinting, and Yuri Dubrova, a Russian geneticist working in Jeffreys’s lab, began to study the effects of Chernobyl after a peculiar experiment they ran in 1992. They subjected male mice to gamma rays and looked at the DNA of their offspring--specifically, at stretches of junk DNA, which rarely produce useful proteins. Junk DNA has a far higher natural mutation rate than functional DNA, which makes changes in the rate easier to detect. Jeffreys and Dubrova discovered that the mutation rate had increased substantially in the offspring of irradiated mice. Somehow the radiation had affected the mouse sperm, and as a result mutations were handed down to future generations.

Wondering how radiation might shuffle junk DNA in humans, Dubrova and Jeffreys got hold of blood samples of 79 families living in contaminated regions in the Mogilev district of Belarus, about 200 miles north of Chernobyl. All the children in the families were born between February and September 1994, some eight years after the accident. Looking for mutations in the younger generation, the researchers compared several stretches of junk DNA in the children with the same stretches in the parents. From this they could estimate an overall mutation rate in the junk DNA. They found that the mutation rate was twice as high in the Belarus children as in a control group of British children.

Those junk-dna mutations, it should be stressed, were not associated with any observed health effects in the Belarus children. Even so, Jeffreys and Dubrova’s finding is important and surprising: studies of Japanese bomb survivors, who were exposed to much higher radiation doses, have never turned up any evidence of inherited mutations. Some experts are thus skeptical of linking the high mutation rate in Belarus to radiation, and Jeffreys himself says the link hasn’t been proved. Belarus is highly polluted in general, which may account for some of the mutation rate. But the rate was significantly higher in families living where cesium 137 contamination was higher, which implicates Chernobyl. And Jeffreys points out that while Japanese survivors received their monstrous radiation dose all at once, Belarus families got theirs over the course of a decade--a pattern that conceivably might produce more mutations. The data can’t be ignored, he concludes.

Especially since similar data were reported this past year from another population living near Chernobyl--a population of rodents. Voles that live in the grasslands around Chernobyl, Robert Baker of Texas Tech and Ronald Chesser of the University of Georgia found, have a rate of DNA mutation at least 100 times higher than voles from a relatively unaffected region 20 miles southeast of Reactor Four. The DNA came from the voles’ mitochondria, which are organelles that supply cells with energy. Such a high mutation rate couldn’t possibly be occurring in the genes of the cell nucleus, as it would almost surely kill the voles. And the Chernobyl voles are anything but dead; although individual voles can set a Geiger counter screaming, the population is thriving.

Similarly, no one knows yet what Chernobyl’s long-term effects on the human population will be--and in particular, whether the high mutation rate in junk DNA implies a high rate in functional genes as well, where mutations can do more damage. The natural mutation rate in such genes is so low that measuring a radiation-induced change is impossible. For Chernobyl’s human victims, the answer may come from epidemiologists, who are monitoring people who don’t want--or can’t afford--to leave their radioactive land; they are also tracking some of the 800,000 Soviet workers who cleaned up the site and built a concrete tomb over the destroyed reactor. The epidemiologists are looking for more cases of thyroid cancer and for other cancers, such as leukemia. Their task is now a grimmer one, for they know that Chernobyl’s final toll may not be assessed in this generation--nor even in the next.